為了提升心肌梗塞患者的組織修復能力和心臟功能，基于骨髓來源細胞通過旁分泌途徑起效的蛋白正日益成為一項核心治療方式。

收集了來自于急性心肌梗塞患者的骨髓來源細胞分泌的蛋白之后，研究者們使用生物信息學方法分析其分秘譜。經過功能性篩選他們發現了一種由C19orf10基因（open reading frame on chromosome 19, 位于第19位染色質的開放閱讀框）編碼的分泌蛋白，而這種蛋白能夠促進心肌細胞的存活和血管新生。研究者們還發現，骨髓來源的單核細胞和巨噬細胞能內源性產生這種蛋白并保護和修復心肌梗塞后的心臟，而且他們將此蛋白命名為髓源性生長因子（MYDGF，myeloid-derived growth factor）。

與野生型小鼠相比，Mydgf基因敲除的小鼠表現出更大的梗塞疤痕以及更嚴重的收縮功能紊亂。而恢復Mydfg基因表達能顯著緩解緊急梗塞之后產生的梗塞疤痕和心肌的收縮功能。此項研究首次報道了髓源性生長因子的生物學功能，并可能作為一種基于功能蛋白的修復缺血組織療法的典型范例。（生物谷世聯博研Bioexcellence）

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Nature Medicine doi:10.1038/nm.3778

Myeloid-derived growth factor (C19orf10) mediates cardiac repair following myocardial infarction

Mortimer Korf-Klingebiel, Marc R Reboll, Stefanie Klede, Torben Brod, Andreas Pich, Felix Polten, L Christian Napp, Johann Bauersachs, Arnold Ganser, Eva Brinkmann, Ines Reimann, Tibor Kempf, Hans W Niessen, Jacques Mizrahi, Hans-Joachim Sch?nfeld, Antonio Iglesias, Maria Bobadilla, Yong Wang & Kai C Wollert

Paracrine-acting proteins are emerging as a central mechanism by which bone marrow cell-based therapies improve tissue repair and heart function after myocardial infarction (MI). We carried out a bioinformatic secretome analysis in bone marrow cells from patients with acute MI to identify novel secreted proteins with therapeutic potential. Functional screens revealed a secreted protein encoded by an open reading frame on chromosome 19 (C19orf10) that promotes cardiac myocyte survival and angiogenesis. We show that bone marrow-derived monocytes and macrophages produce this protein endogenously to protect and repair the heart after MI, and we named it myeloid-derived growth factor (MYDGF). Whereas Mydgf-deficient mice develop larger infarct scars and more severe contractile dysfunction compared to wild-type mice, treatment with recombinant Mydgf reduces scar size and contractile dysfunction after MI. This study is the first to assign a biological function to MYDGF, and it may serve as a prototypical example for the development of protein-based therapies for ischemic tissue repair.